Abstract

Abstract Much attention has been paid to the problem of chronic carriers of Australia antigen [Au(1)] because of the potential transmission of the agent by blood transfusions and by nonparenteral means. Studies from several laboratories have indicated the importance of genetic factors in determining who may become a carrier. Other data have suggested that lymphocyte dysfunction might predispose to persistent Au(1) following infection, and that this may be the susceptibility trait responsible for the existence of many chronic carriers. In order to determine whether impaired lymphocyte function is related to susceptibility to persistence of Au(1), we tested 2 populations living in the same environment, the city of Turin, Italy. One group (Sardinians) has a known high frequency of persistent Au(1) (up to 10 per cent) and was considered a susceptible population. The other (Turinese) has a low frequency (0.5 per cent) and was considered the control population. The study was performed in a series of 14 age- and sex-matched quartets, 2 Sardinians and 2 Turinese, each with and without Au(1). Lymphocyte function was evaluated by culturing the cells with phytohemagglutinin, and quantitating DNA synthesis by measuring the incorporation of 3 H-thymidine and assaying DNA polymerase activity. No differences were found between the Sardinians and Turinese, implying that the lymphocyte deficit is not the basis for susceptibility to persistence of Au(1). The reason for the difference in the frequency of the Au(1) carrier state between the 2 populations remains unknown. Lymphocyte function was also similar in the subjects with and without Au(1), indicatiing that Au(1) per se in a normal host does not impair lymphocyte response. Since such impairment is found in other diseases associated with persistent Au(1) (Down's syndrome, leukemia, Hodgkin's disease, lepromatous leprosy, and chronic renal disease), the lymphocyte abnormality is likely a result of these underlying disorders.

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